β-Amyloid PET and neuropathology in dementia with Lewy bodies

Objective beta -Amyloid (A beta) pathology is common in patients with probable dementia with Lewy bodies (DLB). However, the pathologic basis and the differential diagnostic performance of A beta PET are not established in DLB. Our objective was to investigate the pathologic correlates of C-11-Pittsburgh compound B(PiB) uptake on PET in cases with antemortem diagnosis of probable DLB or Lewy body disease (LBD) at autopsy.MethodsAutopsied cases who underwent antemortem PiB-PET and were assigned a clinical diagnosis of probable DLB or LBD at autopsy were included (n = 39). The primary endpoint was pathologic diagnosis of LBD, Alzheimer disease (AD), or mixed (LBD and AD) pathology; the secondary endpoints included Thal A beta phase and diffuse and neuritic A beta plaques.ResultsLower global cortical PiB standardized uptake value ratio (SUVr) distinguished cases with LBD from cases with AD or mixed pathology with an accuracy of 93%. Greater global cortical PiB SUVr correlated with higher Thal A beta phase (r = 0.75, p <= 0.001). Voxel-based analysis demonstrated that A beta pathology relatively spared the occipital lobes in cases with mixed pathology and LBD compared to cases with AD without LBD, in whom the entire cerebral cortex was involved. Global cortical PiB SUVr was associated primarily with the abundance of diffuse A beta plaques in cases with LBD in a multivariable regression model.ConclusionLower PiB uptake accurately distinguishes cases with LBD from cases with AD or mixed pathology, correlating with the Thal A beta phase. The severity of diffuse A beta pathology is the primary contributor to elevated PiB uptake in LBD.Classification of evidenceThis study provides Class III evidence that lower PiB uptake accurately distinguishes patients with LBD from those with AD or mixed pathology.